Antibodies related idiotypically to the pathogenic antibodies of SLE are produced in normal mice and humans. The production of these antibodies does not lead to the development of disease. The F1 (SNF1) progeny of the cross between a normal, nonautoimmune mouse, SWR and an autoimmune mouse, NZB, develops a severe, and accelerated glomerulonephritis. Immunoglobulin eluted from the renal lesions of SNF 1 mice are related idiotypically (IdLNF 1) related determinants can be produced by the normal SWR parent. The goal of this proposal is to identify any differences in the characteristics or expression of IdLNF 1+ antibodies in the SWR mouse, which distinguishes them from IdLNF 1+antibodies produced in the SNF 1 hybrid. Specifically, the precursor frequency of IdLNF 1+ b cells will be determined in the SWR and SNF 1 hybrid. IdLNF 1+ antibodies derived from unimmunized SWR mice by hybridoma technology will be characterized qualitatively and at the molecular level, to identify differences between these antibodies and IdLNF 1+ antibodies we have previously derived from SNF1 with disease. The kinetics of appearance and specificities of naturally occurring serum IdLNF 1+ antibodies and induced IdLNF 1 antibodies. Regulation of IdLNF 1+ immunoglobulin production by anti-idiotypic antibody and T cells in both strains of mice will be evaluated. The results of these studies will not only add to our understanding of immune regulation, but may help to identify specific mechanisms or defects which lead to the development of autoimmune glomerulonephritis.